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Hyperthyoidism
Anaesthetic Management
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 HYPERTHYROIDISM
Hyperthyroidism and Thyrotoxicosis:
The term hyperthyroidism refers to an inappropriately elevated thyroid function.
The term thyrotoxicosis refers to an excessive amount of circulating thyroid
hormones from any source. Increased levels of thyroid hormones can occur in the
setting of an otherwise normal thyroid function. For example, when there is
inappropriate exogenous thyroid hormone or excessive release of stored
hormone from an inflamed thyroid gland.

Clinical signs and symptoms of hyperthyroidism:

Goiter, tachycardia, anxiety, insomnia, and tremor are seen in over 90% of
patients. Heat intolerance, fatigue, weight loss, ocular signs (proptosis), skeletal
muscle weakness, alopecia, pretibial myxedema, congestive heart failure, and
atrial fibrillation are reported as well
The majority of cases of hyperthyroidism result from one of three pathologic
processes*
 Graves disease,
 toxic multinodular goiter, or a
 toxic adenoma
Regardless of the cause, the signs and symptoms of hyperthyroidism are those of
a hypermetabolic state. The patient is anxious, restless, and hyperkinetic and may
be emotionally unstable. The skin is warm and moist, the face is flushed, the hair
is fine, and the nails are soft and fragile. The patient may demonstrate increased
sweating and complain of heat intolerance.
Associated Endocrine Disorders:
MENtype 2A: Medullary thyroid carcinoma, pheochromocytoma, parathyroid
hyperplasia
MEN type 2B: Medullary thyroid cancer, pheochromocytoma, and growths
around nerves (neuromas).

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MEN I: Pituitary adenoma, parathyroid hyperplasia, pancreatic tumors like
insulinoma and rarely thyroid and adrenal involvement.
Eye signs in hyperthyroidism:
Eyelid retraction ( stare ) (Dalrymple sign): The eyelids are retracted upward
above the superior corneoscleral limbus and the white of the sclera is seen.
Lid-lag (von Graefe’s sign): When the patient tracks an object downward with
their eyes, the eyelid fails to follow the downward moving iris, and the same type
of upper globe exposure which is seen with lid retraction is seen temporarily.
Joffroy’s sign: Absence of wrinkling of the forehead when looking upwards with
the face tilted downwards.
These ocular signs are not the same as exophthalmos (protrusion of the eyeball)
which occurs specifically in Graves’ disease. The forward protrusion of the eyes is
due to immune mediated inflammation in the retro-orbital fat. Exophthalmos
may exacerbate hyperthyroid lid-lag and stare.

Laboratory findings in hyperthyroidism other than TFT:

Hypercalcemia, hypokalemia, hyperglycemia, hypocholesterolemia, mild
anemia, thrombocytopenia, lymphocytosis, granulocytopenia,
hyperbilirubinemia, and increased alkaline phosphatase.

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 Effects of Hyperthyroidism on CVS:
The cardiovascular system is most threatened by hypermetabolism of
peripheral tissues, increased cardiac work with tachycardia, dysrhythmias
(commonly atrial) and palpitations, a hyperdynamic circulation, increased
myocardial contractility and cardiac output, and cardiomegaly. The cardiac
responses are due to the direct effects of T3 on the myocardium and
peripheral vasculature.

Graves disease:
Graves disease, or toxic diffuse goiter, occurs in 0.4% of the US population and
is the leading cause of hyperthyroidism. The disease typically occurs in females
(female/male ratio is 7:1) between the ages of 20 and 40 years.
Although the etiology is unknown, Graves disease appears to be a systemic
autoimmune disease caused by thyroid-stimulating antibodies that bind to TSH
receptors in the thyroid, activating adenylcyclase and stimulating thyroid
growth, vascularity, and hypersecretion of T4 and T3.
The thyroid is usually diffusely enlarged, becoming two to three times its
normal size. An ophthalmopathy occurs in 30% of cases and may include upper
lid retraction, a wide-eyed stare, muscle weakness, proptosis, and an increase
in intraocular pressure. The diagnosis of Graves disease is confirmed by the
presence of thyroid-stimulating antibodies in the context of a low TSH level
and elevated T4 and T3 levels.

Toxic multinodular goiter:

Toxic multinodular goiter usually arises from long-standing simple goiter and
occurs mostly in patients older than age 50. It may present with extreme
thyroid enlargement that can cause dysphagia, globus sensation, and possibly
inspiratory stridor from tracheal compression.
The latter is especially common when the mass extends into the thoracic inlet
behind the sternum. In severe cases, superior vena cava obstruction syndrome
may also be present.
The diagnosis is confirmed by a thyroid scan demonstrating hot patchy foci
throughout the gland or one or two hot nodules. Radioactive iodine uptake

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 and serum T4 and T3 levels may only be slightly elevated. The goiter must be
differentiated from a neoplasm, and a computed tomography (CT) scan and
biopsy may be necessary.

Treatment of hyperthyroidism:
 The first line of treatment for hyperthyroidism is an antithyroid drug,
either methimazole or propylthiouracil (PTU). These agents interfere
with the synthesis of thyroid hormones by inhibiting organification and
coupling.
PTU has the added advantage of inhibiting the peripheral conversion of
T4 to T3. A euthyroid state can almost always be achieved in 6–8 weeks
with either drug if a sufficient dosage is used.
 Iodide in high concentrations inhibits release of hormones from the
hyperfunctioning gland. High concentrations of iodide decrease all
phases of thyroid synthesis and release and result in reduced gland size
and possibly a decrease in vascularity. Its effects occur immediately but
are short-lived.
Therefore iodide is usually reserved for preparing hyperthyroid patients
for surgery, managing patients with actual or impending thyroid storm,
and treating patients with severe thyrocardiac disease.
Iodide is administered orally as a saturated solution of potassium iodide
(SSKI), 3 drops PO every 8 hours for 10–14 days.
Antithyroid drug therapy should precede initiation of iodide treatment,
because administration of iodide alone will increase thyroid hormone
stores and exacerbate the thyrotoxic state.
 Lithium carbonate 300 mg PO every 6 hours may be given in place of
potassium iodide or ipodate to patients who are allergic to iodide
 β-Adrenergic antagonists may relieve signs and symptoms of increased
adrenergic activity such as anxiety, sweating, heat intolerance, tremors,
and tachycardia. Propranolol offers the added features of impairing the
peripheral conversion of T4 to T3.
 Ablative therapy with radioactive iodine 131 or surgery is
recommended for patients with Graves disease.
 Surgery (i.e., subtotal thyroidectomy or possibly total thyroidectomy)
results in prompt control of disease

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Hyperthyroidism in Pregnancy:
Hyperthyroidism during pregnancy is treated with low dosages of antithyroid
drugs. However, these drugs do cross the placenta and can cause fetal
hypothyroidism.
If the mother remains euthyroid while taking small dosages of an antithyroid
drug, the occurrence of fetal hypothyroidism is rare. Radioactive iodine treatment
is contraindicated during pregnancy, as is oral iodide therapy, because it can
cause fetal goiter and hypothyroidism.
Long-term use of propranolol during pregnancy is controversial, since intrauterine
growth retardation has been attributed to its use. Thyroid storm occurring in
pregnancy is managed in the same way as in nonpregnant patients.

Thyroid storm:
Thyroid storm is an acute exacerbation of hyperthyroidism usually caused by a
stress such as surgery or infection. The patients present with hyperthermia,
extreme tachycardia with a high cardiac output, peripheral vasodilation, and
possibly profound hypotension and altered mental state with severe agitation.
Congestive heart failure, dehydration, hyperglycemia, shock, and death also may
occur. Typically, it occurs 6–18 hours postoperatively
It is medical emergency that requires immediate and aggressive management.
Presumptive diagnosis is made on the basis of history and clinical findings

Thyroid storm different from thyrotoxicosis:

Thyroid storm is a severe and life-threatening exacerbation of thyrotoxicosis
usually precipitated by a nonthyroidal illness such as an infection, surgery,
withdrawal of iodine therapy, diabetic ketoacidosis, vigorous palpation of the
thyroid gland, and radioactive iodine therapy.

Differential diagnosis of thyroid storm:

Other Hypermetabolic states:
 Sepsis
 Pheochromocytoma
 cocaine/amphetamine overdose,
 A neuroleptic malignant syndrome in those receiving antipsychotic
medications
 Malignant hyperthermia (MH).

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Treatment of Thyroid strom: First, treat life-threatening changes in vital
signs. Then, make the diagnosis, correct precipitating causes, and treat high
circulating levels of thyroid hormone and resulting effects with beta -blockers
(maintain heart rate <90 beats/min), IV fluids for volume replacement, cooling
and acetaminophen (antipyretic), and antithyroid drugs: propylthiouracil via
nasogastric tube (PTU 600–1,000 mg, followed by 200–400 mg q 8 hourly),
followed 1 hour later by an iodide preparation.
Hydrocortisone (100–200 mg q 8 hourly) has been reported to increase survival.
The duration of storm averages 3 days. Supportive therapy may be needed for
fever, tachycardia, hypotension, volume depletion, hyperglycemia, and altered
consciousness.
Difference between Malignant Hyperthermia and thyroid storm:
Sustained tachycardia, hyperthermia, and increased oxygen consumption are
shared by both. An acute signifi cant elevation in end-tidal CO2, arterial CO2,
metabolic acidosis, and muscle rigidity are features of MH.

Management of Anesthesia:
1) Assesment:
Should be clinically euthyroid, using:
Anti-thyroid drugs orally ( takes 6 weeks)
Lugols Iodine (5% KI ) for 1-2 weeks preop or Na Iodide 500 mg IV q12h
Beta-blockers to control sympathetic nervous system
Occasionally may need alpha-blockers, steroids, sedatives, lithium, etc.

Airway assessment should include:

ENT check of laryngeal nerves ( hoarseness, poor high pitch)
Asessment of postop airway adequacy; tomograms, CT, thoracic inlet XRays;
exclusion of tracheomalacia
Selection of ETT type / size (north rae / reinforced flexible are common choices)

Hypertension, tachycardia, tremor, anxiety, fever, heat intolerance, weight loss,

exophthalmos, myopathy, atrial fibrillation, all suggest poor preoperative control.

2) Anaesthesia Considerations:
Potential difficult airway if goitre present (airway compression, anterior
mediastinal mass)

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 End organ effects of chronic hyperthyroidism:
 Hype eta oli state ↑ VO2, VCO2
 Cardiovascular: hypertension, tachycardia, myocardial ischemia,
cardiomyopathy, arrhythmias
 CNS: anxiety, psychiatric disorders
 Muscle weakness
 Risk of thyroid storm

Interactions with anesthetics:

 ↑ a estheti e ui e e ts
 Avoid sympathetic stimulants (ketamine, cocaine, epinephrine, etc

Thyroidectomy:
Shared airway
Airway obstruction (tracheomalacia, recurrent laryngeal nerve injury, neck
hematoma, hypocalcemia)

3. Optimization:
Optimize thyroid function & limit end organ effects: heart rate <90, normal TSH
Identify difficult airway or anterior mediastinal mass
Identify & manage thyroid storm

4.a Thyroid storm:

 Emergency situation (mortality= 20%), consider endocrinology consult

 IV fluids
 Cool (blankets, IV solution, acetaminophen)
 Control hemodynamics:
Esmolol 0.25-0.5 mg/kg bolus or 50-200 mcg/kg/min infusion
Propranolol 10-40 mg PO or up to 1 mg/min IV
 Stop conversion of T4 to T3:
PTU 200-400 mg PO/NG/PR q6hrly
 Hydrocortisone 100-200 mg IV q8hrly
 Stop synthesis & release of new hormone
Potassium iodide 5 gtts PO/NG q6h or sodium iodide 0.25 g IV q6h (1 hr
after PTU)

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 [Link] for & treat complications:
 CVA, loss of consciousness
 Myocardial infarction, atrial fibrillation (avoid amiodarone because of
iodide content; use digoxin instead) or congestive heart failure
 Hypoventilation & hypercarbia
 Electrolyte abnormalities

C. Consider differential diagnosis for hypermetabolic state

D:Consider last ditch treatments: plasmapheresis, dantrolene,
lithium, neuraxial blockade to T4

Hyperthyroidism - Ten Rules for Anaesthesia Consideration:

1. In hyperthyroid patients undergoing surgery, euthyroidism should definitely be

established preoperatively. In elective cases this may mean waiting a substantial
time (6–8 weeks) for antithyroid drugs to become effective. In emergency cases
the use of a IV β-blocker, ipodate, glucocorticoids, and PTU is usually necessary.
No IV preparation of PTU is available, so the drug must be taken orally, via a
nasogastric tube, or rectally. Glucocorticoids (dexamethasone 2 mg IV every 6
hours) should be administered to decrease hormone release and reduce the
peripheral conversion of T4 to T3.
2. Evaluation of the upper airway for evidence of tracheal compression or
deviation caused by a goiter is an important part of the preoperative evaluation.
Examination of chest radiographs and CT scans is often helpful in this regard.
3. Premedication with anxiolytic, narcotic; reassurance. Intraoperatively the need
for invasive monitoring is determined on an individual basis and depends on the
type of surgery to be performed and the medical condition of the patient. Eye
protection (eyedrops, lubricant, eye pads) is critical, especially for patients with
proptosis.
4. Aim for safe induction with potentially difficult airway - consider fibreoptic,
inhalational, or awake intubation in extreme cases. Test ventilate prior to
nondepolarising relaxant or use suxamethonium and preoxygenation. A
flexometallic tube is preferred when there is tracheal compression and the tube is
placed beyond the length of compression. Drugs that stimulate the sympathetic
nervous system (i.e., ketamine, pancuronium, atropine, ephedrine, epinephrine)
should be avoided.

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5. For maintenance of anesthesia, any of the potent inhalation agents (Isoflurane
and sevoflurane) may be used. Nitrous oxide and opioids (fentanyl)are safe and
effective in hyperthyroid patients. Muscle relaxants (e.g. vecuronium) are guided
by peripheral nerve stimulator. Hyperthyroid patients may have co-existing
muscle disease (e.g., myasthenia gravis) with reduced requirements for the
nondepolarizing muscle relaxants; therefore careful titration is required. If
recurrent laryngeal nerve monitoring is practiced, muscle relaxants are avoided.
6. For treatment of intraoperative hypotension, a direct-acting vasopressor
(phenylephrine) is preferred. Ephedrine, epinephrine, norepinephrine, and
dopamine should be avoided or administered in extremely low doses to prevent
exaggerated hemodynamic responses.
7. Regional anesthesia can be safely performed and in fact may be a preferred
technique. Epinephrine-containing local anesthetic solutions should be avoided.
8. Removal of the thyrotoxic gland does not mean immediate resolution of
thyrotoxicosis. The half-life of T4 is 7–8 days; the efo e β-blocker therapy may
need to be continued in the postoperative period.
9. Carefully monitoring needed for the management of post operative
complications like thyroid storm, airway obstruction, laryngeal nerve damage and
hypocalcemia. Immediate post operative airway obstruction may be due to
oedema ( laryngeal, glottic, supraglottic), haematoma causing external
compression (usually acts via oedema ), RLN damage, hypocalcaemia and tracheal
collapse.
10. For postoperative Analgesia wound infiltration with bupivacaine and
paracetamol and NSAIDs usually are sufficient.

Thyroidectomy patient with respiratory distress D/D:

Vocal cord dysfunction from recurrent laryngeal nerve damage,
cervical hematoma with airway compression,
tracheomalacia, and pneumothorax.

Symptoms of hypocalcemia following thyroidectomy:

Hypoparathyroidism, is usually transient, is main determinant.
Hypocalcemia usually appearing within 72 hours postoperatively; numbness and
tingling around the mouth, hands, and feet; muscle cramps and spasms;
headaches; anxiety; depression.

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Symptomatic hyperthyroidism is scheduled for elective surgery:
Cancel the case and refer the patient to an endocrinologist for preoperative
assessment and preparation.
Treatment includes antithyroid drugs (propylthiouracil, iodine), radioactive iodine,
and surgical subtotal thyroidectomy. If one must proceed, anesthetic risks include
acute exacerbation of hyperthyroidism caused by surgical stress (thyroid storm)
resulting in tachycardia, hyperthermia, hemodynamic instability, and arrhythmia.
Induction with volatile agents is slowed due to the increased cardiac output and
the rate of drug metabolism is increased, with no change in MAC. Emergent cases
should be treated intraoperatively with invasive monitoring, beta-adrenergic
blockade, resuscitation with IV fl uids, and temperature control. Refractory
hypotension from relative cortisol defi ciency may respond to corticosteroids. The
fi rst dose of PTU can be administered down the nasogastric tube. Thyroid storm
usually occurs 6–18 hours after surgery, so the patient should be monitored in a
surgical critical care setting postoperatively.

Ref:
1. Stoelting’s Anesthesia and Co-existing Disease, Seventh edition
2. A. Farling; Thyroid disease, BJA: British Journal of Anaesthesia, Volume 85, Issue
1, 1 July 2000, Pages 15–28
3. Palace MR. Perioperative Management of Thyroid Dysfunction. Health Services
Insights. 2017;10:1178632916689677. doi:10.1177/1178632916689677.

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